The DOI matches its Crossref record; 6 of the 6 references it cites were found in a registry or an index.
Reduced oxidative damage in ALS by high‐dose enteral melatonin treatment
Open accessAbstract
Abstract: Amyotrophic lateral sclerosis (ALS) is the collective term for a fatal motoneuron disease of different etiologies, with oxidative stress as a common molecular denominator of disease progression. Melatonin is an amphiphilic molecule with a unique spectrum of antioxidative effects not conveyed by classical antioxidants. In preparation of a possible future clinical trial, we explored the potential of melatonin as neuroprotective compound and antioxidant in: (1) cultured motoneuronal cells (NSC‐34), (2) a genetic mouse model of ALS (SOD1 G93A‐transgenic mice), and (3) a group of 31 patients with sporadic ALS. We found that melatonin attenuates glutamate‐induced cell death of cultured motoneurons. In SOD1 G93A‐transgenic mice, high‐dose oral melatonin delayed disease progression and extended survival. In a clinical safety study, chronic high‐dose (300 mg/day) rectal melatonin was well tolerated during an observation period of up to 2 yr. Importantly, circulating serum protein carbonyls, which provide a surrogate marker for oxidative stress, were elevated in ALS patients, but were normalized to control values by melatonin treatment. This combination of preclinical effectiveness and proven safety in humans suggests that high‐dose melatonin is suitable for clinical trials aimed at neuroprotection through antioxidation in ALS.
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Cites
Of Mice and Not Men: Differences between Mouse and Human Immunology
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Trk Receptors: Roles in Neuronal Signal Transduction
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“Similarly, Western blot analysis of spinal cord protein lysates failed to detect differences in total amount or phosphorylation status of AKT or ERK1/2, kinases involved in the modulation of neuronal cell death [34].”
Backgroundβ-Lactam antibiotics offer neuroprotection by increasing glutamate transporter expression
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Development and characterisation of a glutamate-sensitive motor neurone cell line
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Cited by
Oxidative Stress in Neurodegenerative Diseases
Simonian, N. A., & Coyle, J. T. (1996) · Annual Review of Pharmacology and Toxicology · doi:10.1146/annurev.pa.36.040196.000503 · Cited by 1,377
Autophagy and apoptosis dysfunction in neurodegenerative disorders
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Melatonin—A pleiotropic, orchestrating regulator molecule
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Self-citationOxidative Stress in Neurodegenerative Diseases
Niedzielska, E., Smaga, I., Gawlik, M., Moniczewski, A., Stankowicz, P., Pera, J., & Filip, M. (2016) · Molecular Neurobiology · doi:10.1007/s12035-015-9337-5 · Cited by 800
Update on melatonin receptors: IUPHAR Review 20
Jockers, R., Delagrange, P., Dubocovich, M. L., Markus, R. P., Renault, N., Tosini, G., Cecon, E., & Zlotos, D. P. (2016) · British Journal of Pharmacology · doi:10.1111/bph.13536 · Cited by 422
Metadata
- Authors
- Weishaupt, J. H., Bartels, C., Pölking, E., Dietrich, J., Rohde, G., Poeggeler, B., Mertens, N., Sperling, S., Bohn, M., Hüther, G., Schneider, A., Bach, A., Sirén, A., Hardeland, R., Bähr, M., Nave, K., & Ehrenreich, H.
- Venue
- Journal of Pineal Research
- Publisher
- Wiley
- Published
- 2006-08-29
- Volume
- 41
- Issue
- 4
- Pages
- 313-323
- ISSN
- 0742-3098 (ISSN-L)
- 1600-079X
- OpenAlex
- W2113208927
- Cited by
- 282
- References
- 6
- FWCI
- 6.48
- Type
- journal article
- Language
- en
- Open access
- bronze
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- Weishaupt, J. H., Bartels, C., Pölking, E., Dietrich, J., Rohde, G., Poeggeler, B., Mertens, N., Sperling, S., Bohn, M., Hüther, G., Schneider, A., Bach, A., Sirén, A., Hardeland, R., Bähr, M., Nave, K., & Ehrenreich, H. (2006). Reduced oxidative damage in ALS by high‐dose enteral melatonin treatment. Journal of Pineal Research. https://doi.org/10.1111/j.1600-079x.2006.00377.x
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
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